摘要
目的明确丹参酮ⅡA(TanⅡA)是否能够减轻人脐静脉内皮细胞(HUVEC)损伤,以及其作用机制是否与调节氧化应激有关。方法以高糖诱导的损伤HUVEC作为细胞模型,在体外环境下探讨TanⅡA的作用。实验中采用CCK-8细胞活性检测明确细胞活性的变化;Western blot实验探讨P38、p-P38、caspase 3、cleaved caspase 3等蛋白表达的变化;活性氧/超氧阴离子(ROS/O_(2)^(-))荧光探针检测各组细胞ROS、O_(2)^(-)表达的变化。结果高糖可诱导HUVEC活性下降,ROS、O_(2)^(-)表达明显增加,p-P38、cleaved caspase 3蛋白表达明显上升。而TanⅡA可减轻高糖诱导的HUVEC活性的下降,抑制ROS、O_(2)^(-)升高,抑制P38的磷酸化以及caspase 3的活化。结论高糖可诱导HUVEC凋亡,而TanⅡA通过抑制ROS/P38 MAPK信号通路减轻高糖诱导的HUVEC凋亡。
Objective To determine the effects of tanshinoneⅡA(TanⅡA)on the injury of human umbilical vein endothelial cells(HUVECs),and its relationship with oxidative stress regulation.Methods HUVECs were cultured in high glucose medium to investigate the role of TanⅡA in vitro.The cell viability was measured by CCK-8 assay.The levels of P38,p-P38,caspase 3 and cleaved caspase 3 were investigated by Western blot.Reactive oxygen species/superoxide anion(ROS/O-2)fluorescence probe was used to detect the changes of ROS and O-2 in each group.Results High glucose treatment induced decreased HUVECs viability,enhanced the expression of ROS and O-2,and increased the levels of p-P38 and cleaved caspase 3.Furthermore,exposure to TanⅡA resulted in decreases in HUVEC viability induced by high glucose,inhibited the expressions of ROS and O-2,and blocked P38 phosphorylation and the activation of caspase 3.Conclusions High glucose can cause apoptosis in HUVECs,and TanⅡA can relieve HUVECs apoptosis induced by high glucose through inhibiting the ROS/P38 MAPK signaling pathway.
作者
蒋诗敏
张珂嘉
周泰
周瑶
李俐
JIANG Shimin;ZHANG Kejia;ZHOU Tai;ZHOU Yao;LI Li(Department of Pathophysiology,Xuzhou Medical University,Xuzhou,Jiangsu 221004,China;Department of Pathology,Xuzhou Medical University)
出处
《徐州医科大学学报》
CAS
2021年第4期235-240,共6页
Journal of Xuzhou Medical University
基金
国家自然科学基金青年项目(82004107)
徐州医科大学优秀人才科研启动基金(D2019016)。
关键词
丹参酮
糖尿病
氧化应激
细胞凋亡
tanshinoneⅡA
diabetes
oxidative stress
cell apoptosis
